ABSTRACT
Abstract Purpose To investigate the protective effect of Ganoderma lucidum on testicular torsion/detorsion (T/D)-induced ischemia-reperfusion (I/R) injury. Methods Thirty male Wistar albino rats were randomly categorized into 3 groups: Group 1: sham, Group 2 ( T/D): 2,5 hours of ischemia and 7 days of reperfusion, Group 3 (T/D+ G. lucidum ): 2,5 hours of ischemia and 7 days of reperfusion and 7 days of 20 mg/kg via gastric gavage G. lucidum polysaccharides per day. Biochemical assays of Malondialdehyde (MDA), superoxide dismutase (SOD), Catalase (CAT), Glutathione (GSH) levels , histopathology and expression levels of VEGF and Bcl-2 with immunohistochemical methods were examined in testicular tissue. Results G. lucidum treatment was found to have prevented the T/D-induced I/R injury by decreasing MDA levels of the testis. SOD, CAT and GSH activities were decreased in group 2, while they were increased in group 3 (p<0.001) and significant improvement in the tube diameter was observed in group 3. Bcl-2-positive germinal cells were lowered in group 3 compared to the group 2. VEGF expression showed an increase in group 2, whereas it decreased in group 3. Conclusion The antioxidant G. lucidum is thought to induce angiogenesis by reducing the apoptotic effect in testicular torsion-detorsion.
Subject(s)
Animals , Male , Rats , Spermatic Cord Torsion/complications , Testis/blood supply , Reperfusion Injury/prevention & control , Reishi/chemistry , Antioxidants/therapeutic use , Spermatic Cord Torsion/metabolism , Superoxide Dismutase/metabolism , Testis/drug effects , Testis/pathology , Reperfusion Injury/etiology , Catalase/metabolism , Random Allocation , Rats, Wistar , Vascular Endothelial Growth Factor A/metabolism , Drug Evaluation, Preclinical , Malondialdehyde/metabolism , Antioxidants/pharmacologyABSTRACT
Abstract Purpose: Ganoderma lucidum, a kind of mushroom used for its antioxidant, anti-inflammatory, and immunomodulatory activities, was investigated in the present study for its possible healing effect on calvarial defects with bone grafts. Methods: Wistar male rats (n = 30) were divided into 3 groups: 1) the control (defect) group (n = 10), 2) defect and graft group (n = 10), and 3) defect, graft, and G. lucidum treated group (n = 10). The G. lucidum was administered to the rats at 20 mL/kg per day via gastric lavage. Results: In the defect and graft group, osteonectin positive expression was observed in osteoblast and osteocyte cells at the periphery of the small bone trabeculae within the graft area. In the defect, graft, and G. lucidum treated group, osteonectin expression was positive in the osteoblast and osteocyte cells and positive osteonectin expression in new bone trabeculae. The expression of matrix metalloproteinase-9 (MMP-9) was positive in the inflammatory cells, fibroblast cells, and degenerated collagen fibril areas within the defect area. Conclusion: This study shows that, with its antioxidant and anti-inflammatory properties, G. Lucidum is an important factor in the treatment of calvarial bone defects.
Subject(s)
Animals , Male , Rats , Skull/surgery , Bone Regeneration/drug effects , Bone Transplantation , Reishi/chemistry , Anti-Inflammatory Agents/therapeutic use , Antioxidants/therapeutic use , Skull/drug effects , Immunohistochemistry , Osseointegration/drug effects , Rats, Wistar , Disease Models, AnimalABSTRACT
Traumatic brain injury (TBI) can potentially lead to hemorrhages in all areas of the skull, which can damage cells and nerve connections. This study aims to investigate the protective effects of Ganoderma lucidum polysaccharides (GLPS) as a antioxidant on cerebellar cell tissues after traumatic brain injury in rats. Sprague Dawley rats were subjected to TBI with a weight-drop device using 300 g1m weight-height impact. The groups are consisted of control, trauma, and trauma+Ganoderma lucidum groups. At seven days post-brain injury, experimental rats were decapitated after intraperitoneal administration of ketamine HCL (0.15 ml/100 g body weight). Cereballar samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) activity. Significant improvement was observed in cells and vascular structures of Ganoderma lucidum treated groups when compared to untreated groups. It is believed that Ganoderma lucidum may have an effect on the progression of traumatic brain injury. Ganoderma lucidum application may affect angiogenetic development in blood vessel endothelial cells, decrease inflammatory cell accumulation by affecting cytokine mechanism and may create apoptotic nerve cells and neuroprotective mechanism in glial cells.
La lesión cerebral traumática (LCT) puede provocar hemorragias en todas las áreas del cráneo, lo que puede dañar las células y las conexiones nerviosas. Este estudio tuvo como objetivo investigar los efectos protectores de los polisacáridos de Ganoderma lucidum (GLPS) como antioxidante en los tejidos de las células del cerebelo después de la lesión cerebral traumática en ratas. Ratas Sprague Dawley fueron sometidas a TBI con un dispositivo de caída de peso usando un impacto de peso de 300 g-1 m. Se formaron los siguientes grupos: control, trauma y trauma + Ganoderma lucidum. Siete días después de la lesión cerebral, las ratas experimentales fueron decapitadas después de la administración intraperitoneal de ketamina HCL (0,15 ml / 100 g de peso corporal). Se tomaron muestras cerebrales para el examen histológico y para la determinación de niveles de malondialdehído (MDA) y glutatión (GSH) y actividad de mieloperoxidasa (MPO). Se observó una mejora significativa en las células y las estructuras vasculares de los grupos tratados con Ganoderma lucidum en comparación con los grupos no tratados. Durante el estudio se observó que Ganoderma lucidum puede tener un efecto sobre la progresión de la lesión cerebral traumática. La aplicación de Ganoderma lucidum puede afectar el desarrollo angiogénico en las células endoteliales de los vasos sanguíneos, disminuir la acumulación de células inflamatorias al afectar el mecanismo de las citocinas y puede crear células nerviosas apoptóticas y un mecanismo neuroprotector en las células gliales.
Subject(s)
Animals , Male , Rats , Cerebellum/drug effects , Reishi/chemistry , Brain Injuries, Traumatic/pathology , Antioxidants/pharmacology , Polysaccharides/pharmacology , Immunohistochemistry , Antigens, Differentiation, Myelomonocytic , Antigens, CD , Cerebellum/metabolism , Cerebellum/pathology , Blotting, Western , Rats, Sprague-Dawley , Peroxidase/metabolism , Neuroprotective Agents , Proto-Oncogene Proteins c-bcl-2 , Vascular Endothelial Growth Factor A/metabolism , Glutathione/analysis , Malondialdehyde/analysisABSTRACT
SUMMARY: Traumatic injury to the spinal cord results in the delayed dysfunction and neuronal death. Impaired mitochondrial function, generation of reactive oxygen species (ROS), and lipid peroxidation occur soon after traumatic spinal cord injury (SCI), while the activation of compensatory molecules that neutralize ROS occurs at later time points. The aim of the current study was to investigate the putative neuroprotective effect of Ganoderma lucidum in a rat model of SCI. In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10, was used. Injured animals were given either 20 mL/kg Ganoderma lucidum or saline 30 min post injury per day by gastric gavage. At seven days postinjury, rats were decapitated. Spinal cord samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity. SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in MDA levels, MPO activity. On the other hand, Ganoderma lucidum treatment reversed all these biochemical parameters as well as SCI-induced histopathological alterations. Furthermore, impairment of the neurological functions due to SCI was improved by meloxicam treatment. The present study suggests that Ganoderma Lucidum, reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, GSH depletion.
RESUMEN: La lesión traumática de la médula espinal provoca disfunción retrasada y muerte neuronal. La función mitocondrial deteriorada, la generación de especies reactivas de oxígeno (ERO) y la peroxidación lipídica ocurren poco después de una lesión traumática de la médula espinal (LTE), mientras que la activación de moléculas compensatorias que neutralizan ERO ocurre posteriormente. El objetivo del presente estudio fue investigar el efecto neuroprotector de Ganoderma lucidum en un modelo de LTE en ratas. Con el fin de inducir LTE, se utilizó un método estándar de pérdida de peso que indujo una lesión moderadamente grave (100 g / cm de fuerza) a T10. A los animales lesionados se les administró 20 ml / kg de Ganoderma lucidum o solución salina, por sonda gástrica, 30 minutos después de la lesión. A los siete días después de la lesión, las ratas fueron eutanasiadas por decapitación. Se tomaron muestras de médula espinal para el examen histológico y para la determinación de los niveles de malondialdehído (MDA) y glutatión (GSH), y la actividad de mieloperoxidasa (MPO). LTE causó una disminución significativa en el contenido de GSH de la médula espinal, además de aumentos significativos en los niveles de MDA y la actividad de MPO. Por otro lado, el tratamiento con Ganoderma lucidum invirtió todos estos parámetros bioquímicos así como las alteraciones histopatológicas inducidas por LTE. El deterioro de las funciones neurológicas debidas a LTE mejoró con el tratamiento con meloxicam. El presente estudio sugiere que Ganoderma lucidum, reduce el estrés oxidativo inducido por LTE y ejerce la neuroprotección mediante la inhibición de la peroxidación de los lípidos y agotamiento del GSH.
Subject(s)
Animals , Rats , Neuroprotective Agents/administration & dosage , Reishi/chemistry , Spinal Cord Injuries/drug therapy , Glutathione/analysis , Immunohistochemistry , In Situ Nick-End Labeling , Malondialdehyde/analysis , Oxidative Stress/drug effects , Peroxidase/drug effects , Rats, Sprague-Dawley , Spinal Cord Injuries/pathologyABSTRACT
Head trauma affects the optic nerve visual function and visual acuity. As a result of head trauma occurring in the retina of the various biochemical, histological and immunohistochemical effects were investigated. The protective effect of Ganoderma lucidum was evaluated on the damage to the retina of the rats. Sprague-Dawley rats were subjected to traumatic brain injury with a weight-drop device using 300 g-1 m weight-height impact. Thirty rats were divided into three groups as group 1 control, 2 group trauma, 3 group trauma+Gonoderma lucidum (20 mL/kg per day via gastric gavage) Ganoderma lucidum was administered for 7 days after trauma.All rats were decapitated 5 days after the induction of trauma, and the protective effects of Ganoderma lucidum in retina were evaluated by histological, immunohistochemical and biochemical analyses. The antioxidant effect of Ganoderma lucidum on the cellular degeneration extracellular matrix and retinal barrier in retina after head trauma was investigated.
El traumatismo craneal afecta al nervio óptico en relación a su función y la agudeza visual. Se estudiaron los diversos efectos bioquímicos, histológicos e inmunohistoquímicos en la retina producidos por una lesión y trauma a la cabeza. En esta investigación se evaluó el efecto protector de Gonaderin lucidum sobre el daño a la retina de ratas. Ratas Sprague-Dawley fueron sometidas a una lesión cerebral traumática con un dispositivo de caída de peso usando un impacto de 300 g-1 m de peso-altura. Treinta ratas se dividieron en tres grupos: grupo 1, de control; grupo 2, trauma; grupo 3, de trauma + Gonoderma lucidum (20 ml / kg día, a través de una sonda gástrica). Ganoderma lucidum se administró durante 7 días después del trauma. Todas las ratas fueron decapitadas 5 días después. La inducción del trauma y los efectos protectores de Ganoderma lucidum en la retina fueron evaluados mediante análisis histológicos, inmunohistoquímicos y bioquímicos. Se investigó el efecto antioxidante de Ganoderma lucidum sobre la degeneración celular en la matriz extracelular y la barrera retiniana en la retina después del traumatismo craneal.
Subject(s)
Animals , Male , Rats , Antioxidants/administration & dosage , Craniocerebral Trauma/pathology , Plant Extracts/administration & dosage , Reishi/chemistry , Retinal Diseases/drug therapy , Antioxidants/metabolism , Craniocerebral Trauma/drug therapy , Immunohistochemistry , Plant Extracts/metabolism , Rats, Sprague-Dawley , Retinal Diseases/etiology , Retina/pathologyABSTRACT
El hongo Ganoderma lucidum, en los constituyentes de su biomasa, tiene compuestos con propiedades benéficas para la salud; es por esto que el conocimiento de las condiciones nutricionales adecuadas para su crecimiento permitirá su producción industrial y a bajo costo. En este trabajo se evaluó a nivel de matraz el efecto de la relación C/N, y la presencia de diferentes fuentes de carbono, nitrógeno y micronutrientes sobre la producción de biomasa. Empleando glucosa y peptona como fuentes de carbono y nitrógeno, respectivamente, se encontró una relación C/N óptima de 16,7:1 para la cual la máxima producción de biomasa fue de 25 g/L. Manteniendo esta relación C/N, y sustituyendo la glucosa por lactosa o harina de cebada y la peptona por extracto de levadura, la producción de biomasa se incrementó a 35 g/L. En presencia de harina de cebada la adición al medio de cultivo de sales de Mg y K, y de tiamina, no generó un mayor incremento en la producción de biomasa. La producción de biomasa de G. lucidum se ve favorecida por la presencia en el medio de cultivo de relaciones C/N cercanas a las reportadas conforme a la composición típica de los hongos, así como por la presencia de sustratos complejos como la harina de cebada que le aportan además de la fuente de carbono micronutrientes necesarios para su desarrollo.
Ganoderma lucidum fungus has some biomass components with beneficial health properties. The knowledge about its nutritionals requirements for growing will favor its industrial production at lower cost. In this work, the effect of C/N ratio, the presence of different carbon, nitrogen and micronutrients sources, on fungal biomass production, were evaluated. Using glucose and peptone as carbon and nitrogen sources, respectively, an optimal C/N ratio of 16,7:1 was found, for which the maximal biomass production was 25 g/L. Replacing glucose by lactose or barley flour and peptone by yeast extract at the same C/N ratio, the biomass production was enhanced to 35 g/L. With barley flour in the culture medium, the presence of Mg and K salts and thiamine did not turn out into a major increase of biomass. The G. lucidum biomass production is promoted by C/N ratios in the culture medium nearly equivalent to that found in the fungus, as well as the presence of complex substrates as barley flour which, additionally, contributes with important micronutrients along with the carbon source.
Subject(s)
Micronutrients/analysis , Micronutrients/biosynthesis , Micronutrients/pharmacokinetics , Micronutrients/pharmacology , Micronutrients/physiology , Micronutrients/genetics , Micronutrients/immunology , Micronutrients/metabolism , Micronutrients/chemistry , Micronutrients/chemical synthesis , Biomass , Reishi/isolation & purification , Reishi/physiology , Reishi/genetics , Reishi/chemistryABSTRACT
The fungal beta-D-glucan is a biological response modifier (BRM), but a major obstacle to the clinical utilization of beta-glucan BRMs is thei relative lack of solubility in aqueous media. Water insoluble fungal glucans extracted by alkali from the mycelia of Ganoderma lucidum were sulfated to yield their corresponding water-soluble derivatives. Insoluble glucan is dissolved in methyl sulfoxide and urea, and is partially sulfated with sulfuric acid. The sulfated glucan (SGL) yield prepared from insoluble glucan (IGL) was 85%, the sulfation degree of SGL was about 14.9%, and the solubility of SGL was above 95% in water. The monosugar SGL content was 34.9% alpha-glucose and 35.9% beta-glucose. The mean molecular weight (MW) of SGL was shown as a single peak on Sepharose CL-4B column chromatography, and their MW was approximately 9.3 kDa. The 13C NMR spectrum analysis shows that SGL has a high similarity with the beta-(1-->3)-linked triple-helical control.